The China Study (7 page)

34                            THE CHINA STUDY
make their children well, they would not have to rely on scarce medicines
and the mostly nonexistent doctors. Engel started the program in 1967
and invited me to be his Campus Coordinator and to come for extended
stays in the Philippines while he resided full time in Manila.
Consistent with the emphasis on protein as a means of solving mal-
n u t r i t i o n , we had to make this nutrient the centerpiece of our educa-
tional "mothercraft" centers and thereby help to increase protein con-
s u m p t i o n . Fish as a source of protein was mostly limited to the seacoast
areas. Our own preference was to develop peanuts as a source of protein
because this was a crop that could be grown most anywhere. The peanut
is a legume, like alfalfa, soybeans, clover, peas and other beans. Like
these other nitrogen "fixers," peanuts are rich in protein.
There was, however, a nagging problem with these tasty legumes.
Considerable evidence had been emerging, first from England7- 9 and
later from MIT (the same lab that I had worked in) 10, 11 to show that pea-
n u t s often were contaminated with a fungus-produced toxin called af-
latoxin (AF). It was an alarming problem because AF was being shown
to cause liver cancer in rats. It was said to be the most potent chemical
carcinogen ever discovered.
So we had to tackle two closely related projects: alleviate childhood
malnutrition and resolve the AF contamination problem.
Prior to going to the Philippines, I had traveled to Haiti in order to
observe a few experimental mothercraft centers organized by my col-
leagues at Virginia Tech, Professors Ken King and Ryland Webb. It was
my first trip to an underdeveloped country, and Haiti certainly fit the
bill. Papa Doc Duvalier, president of Haiti, extracted what little resourc-
es the country had for his own rich lifestyle. In Haiti at that time 54%
of the children were dead before reaching their fifth birthday, largely
because of malnutrition.
I subsequently went to the Philippines and encountered more of the
same. We decided where mothercraft centers were to be located based
on how much malnutrition was present in each village. We focused our
efforts on the villages in most need. In a preliminary survey in each vil-
lage (barrio), children were weighed and their weight for age was com-
p a r e d with a Western reference standard, which was subdivided into
first, second and third degree malnutrition. Third degree malnutrition,
the worst kind, represented children under the 65 th percentile. Keep in
mind that a child at the lOOth percentile represents only the average for
the u.s. Being less than the 65 th percentile means near starvation.

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In the urban areas of some of the big cities, as many as 15-20% of
the children aged three to six years were judged to be third degree. I
can so well remember some of my initial observations of these children.
A mother, hardly more than a wisp herself, holding her three-year-old
twins with bulging eyes, one at eleven pounds, the other at fourteen
pounds, trying to get them to open their mouths to eat some porridge.
Older children blind from malnutrition, being led around by their
younger siblings to seek a handout. Children without legs or arms hop-
ing to get a morsel of food.
A REVELATION TO DIE FOR
Needless to say, those sights gave us ample motivation to press ahead
with our project. As I mentioned before, we first had to resolve the
problem of AF contamination in peanuts, our preferred protein food.
The first step of investigating AF was to gather some basic information.
Who in the Philippines was consuming AF, and who was subject to liver
cancer? To answer these questions, I applied for and received a National
Institutes of Health (NIH) research grant. We also adopted a second strat-
egy by asking another question: how does AF actually affect liver cancer?
We wanted to study this question at the molecular level using laboratory
rats. I succeeded in getting a second NIH grant for this in-depth bio-
chemical research. These two grants initiated a two-track research inves-
tigation, one basic and one applied, which was to continue for the rest of
my career. I found studying questions both from the basic and applied
perspectives rewarding because it tells us not only the impact of a food
or chemical on health, but also why it has that impact. In so doing, we
could better understand not only the biochemical foundation of food and
health, but also how it might relate to people in everyday life.
We began with a stepwise series of surveys. First, we wanted to know
which foods contained the most AF. We learned that peanuts and corn
were the foods most contaminated. All twenty-nine jars of peanut butter
we had purchased in the local groceries, for example, were contami-
nated, with levels of AF as much as 300 times the amount judged to be
acceptable in U.s. food. Whole peanuts were much less contaminated;
none exceeded the AF amounts allowed in U.s. commodities. This
disparity between peanut butter and whole peanuts originated at the
peanut factory. The best peanuts, which filled "cocktail" jars, were hand
selected from a moving conveyor belt, leaving the worst, moldiest nuts
to be delivered to the end of the belt to make peanut butter.

THE CHINA STUDY
36
Our second question concerned who was most susceptible to this AF
contamination and its cancer-producing effects. We learned that it was
children. They were the ones consuming the AF-Iaced peanut butter.
We estimated AF consumption by analyzing the excretion of AF meta-
bolic products in the urine of children living in homes with a partially
consumed peanut butter jar. 12 As we gathered this information an inter-
esting pattern emerged: the two areas of the country with the highest
rates of liver cancer, the cities of Manila and Cebu, also were the same
areas where the most AF was being consumed. Peanut butter was almost
exclusively consumed in the Manila area while corn was consumed in
Cebu, the second most populated city in the Philippines.
But, as it turned out, there was more to this story. It emerged from my
making the acquaintance of a prominent doctor, Dr. Jose Caedo, who
was an advisor to President Marcos. He told me that the liver cancer
problem in the Philippines was quite serious. What was so devastating
was that the disease was claiming the lives of children before the age of
ten. Whereas in the West, this disease mostly strikes people only after
forty years of age, Caedo told me that he had personally operated on
children younger than four years of age for liver cancer!
That alone was incredible, but what he then told me was even more
striking. Namely, the children who got liver cancer were from the best-fed
families. The families with the most money ate what we thought were
the healthiest diets, the diets most like our own meaty American diets.
They consumed more protein than anyone else in the country (high quality
animal protein, at that), and yet they were the ones getting liver cancer!
How could this be? Worldwide, liver cancer rates were highest in
countries with the lowest average protein intake. It was therefore widely
believed that this cancer was the result of a deficiency in protein. Fur-
ther, the deficiency problem was a major reason we were working in the
Philippines: to increase the consumption of protein by as many mal-
n o u r i s h e d children as possible. But now Dr. Caedo and his colleagues
were telling me that the most protein-rich children had the highest rates
of liver cancer. This seemed strange to me, at first, but over time my
own information increasingly confirmed their observations.
At that time, a research paper from India surfaced in an obscure med-
ical journal. 13 It was an experiment involving liver cancer and protein
consumption in two groups of laboratory rats. One group was given AF
and then fed diets containing 20% protein. The second group was given
the same level of AF and then fed diets containing only 5% protein.

37
A HOUSE OF PROTEINS
Every single rat fed 20% protein got liver cancer or its precursor lesions,
but not a single animal fed a 5% protein diet got liver cancer or its pre-
c u r s o r lesions. It was not a trivial difference; it was 100% versus 0%.
This was very much consistent with my observations for the Philippine
children. Those who were most vulnerable to liver cancer were those
who consumed diets higher in protein.
No one seemed to accept the report from India . On a flight from De-
troit after returning from a presentation at a conference, I traveled with
a former but much senior colleague of mine from MIT, Professor Paul
Newberne. At the time, Newberne was one of the only people who had
given much thought to the role of nutrition in the development of can-
cer. I told him about my impressions in the Philippines and the paper
from India. He summarily dismissed the paper by saying, "They must
have gotten the numbers on the animal cages reversed. In no way could
a high-protein diet increase the development of cancer. "
I realized that I had encountered a provocative idea that stimulated
disbelief, even the ire of fellow colleagues. Should I take seriously the
observation that protein increased cancer development and run the risk
of being thought a fool? Or should I turn my back on this story?
In some ways it seemed that this moment in my career had been fore-
s h a d o w e d by events in my personal life. When I was five years old, my
aunt who was living with us was dying of cancer. On several occasions
my uncle took my brother Jack and me to see his wife in the hospital.
Although I was too young to understand everything that was happen-
ing, I do remember being struck by the big " C ' word: cancer. I would
think, "When I get big, I want to find a cure for cancer. "
Many years later, just a few years after getting married, at about the
time when I was starting my work in the Philippines, my wife's mother
was dying of colon cancer at the young age of fifty-one. At that time, I
was becoming aware of a possible diet-cancer connection in our early
research. Her case was particularly difficult because she did not receive
appropriate medical care due to the fact that she did not have health
insurance. My wife Karen was her only daughter and they had a very
close relationship. These difficult experiences were making my career
choice easy: I would go wherever our research led me to help get a bet-
ter understanding of this horrific disease.
Looking back on it, this was the beginning of my career focus on diet
and cancer. The moment of deciding to investigate protein and cancer
was the turning point. If I wanted to stay with this story, there was only

38                           THE CHINA STUDY
one solution: start doing fundamental laboratory research to see not only
if, but also how, consuming more protein leads to more cancer. That's
exactly what I did. It took me farther than I had ever imagined. The ex-
traordinary findings my colleagues, students and I generated just might
make you think twice about your current diet. But even more than that,
the findings led to broader questions, questions that would eventually
lead to cracks in the very foundations of nutrition and health.
THE NATURE OF SCIENCE-WHAT YOU NEED TO KNOW
TO FOLLOW THE RESEARCH
Proof in science is elusive. Even more than in the "core" sciences of biol-
ogy, chemistry and physics, establishing absolute proof in medicine and
health is nearly impossible. The primary objective of research investiga-
tion is to determine only what is likely to be true. This is because research
into health is inherently statistical. When you throw a ball in the air, will
it come down? Yes, every time. That's physics. If you smoke four packs a
day, will you get lung cancer? The answer is maybe. We know that your
odds of getting lung cancer are much higher than if you didn't smoke, and
we can tell you what those odds (statistics) are, but we can't know with
certainty whether you as an individual will get lung cancer.
In nutrition research, untangling the relationship between diet and
health is not so straightforward. Humans live all sorts of different ways,
have different genetic backgrounds and eat all sorts of different foods.
Experimental limitations such as cost restraints, time constraints and
measurement error are significant obstacles. Perhaps most importantly,
food, lifestyle and health interact through such complex, multifaceted
systems that establishing proof for anyone factor and anyone disease is
nearly impossible, even if you had the perfect set of subjects, unlimited
time and unlimited financial resources.
Because of these difficulties, we do research using many different
strategies. In some cases, we assess whether a hypothetical cause pro-
duces a hypothetical effect by observing and measuring the differences
that already exist between different groups of people. We might observe
and compare societies who consume different amounts of fat, then ob-
serve whether these differences correspond to similar differences in the
rates of breast cancer or osteoporosis or some other disease condition.
We might observe and compare the dietary characteristics of people who
already have the disease with a comparable group of people who don't
have the disease. We might observe and compare disease rates in 1950

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with disease rates in 1990, then observe whether any changes in disease
rates correspond to dietary changes.
In addition to observing what already exists, we might do an experi-
m e n t and intentionally intervene with a hypothetical treatment to see
what happens. We intervene, for example, when testing for the safety
and efficacy of drugs. One group of people is given the drug and a sec-
o n d group a placebo (an inactive look-alike substance to please the
patient) . Intervening with diet, however, is far more difficult, especially
if people aren't confined to a clinical setting, because then we must rely
on everyone to faithfully use the specified diets.
As we do observational and interventional research, we begin to amass
the findings and weigh the evidence for or against a certain hypothesis.
When the weight of the evidence favors an idea so strongly that it can no
longer be plausibly denied, we advance the idea as a likely truth. It is in
this way that I am advancing an argument for a whole foods, plant-based
diet. As you continue reading, realize that those seeking absolute proof
of optimal nutrition in one or two studies will be disappointed and con-
fused. However, I am confident that those seeking the truth regarding diet
and health by surveying the weight of the evidence from the variety of
available studies will be amazed and enlightened. There are several ideas
to keep in mind when determining the weight of the evidence, including
the following ideas.
CORRELATION VERSUS CAUSATION
In many studies, you will find that the words correlation and association
are used to describe a relationship between two factors, perhaps even in-
dicating a cause-and-effect relationship. This idea is featured prominently
in the China Study: We observed whether there were patterns of associa-
tions for different dietary, lifestyle and disease characteristics within the
survey of 65 counties, 130 villages and 6,500 adults and their families.
If protein consumption, for example, is higher among populations that
have a high incidence of liver cancer, we can say that protein is positively
correlated or associated with liver cancer incidence; as one goes up, the
other goes up. If protein intake is higher among populations that have a
low incidence of liver cancer, we can say that protein is inversely associ-
ated with liver cancer incidence. In other words, the two factors go in the
opposite direction; as one goes up, the other goes down.
In our hypothetical example, if protein is correlated with liver can-
cer incidence, this does not prove that protein causes or prevents liver